Harrisons Manual of Medicine, 18th Ed.

CHAPTER 33. Bioterrorism


Microbial bioterrorism refers to the use of microbial pathogens as weapons of terror that target civilian populations. A primary goal of bioterrorism is not necessarily to produce mass casualties but to destroy the morale of a society through creating fear and uncertainty. The events of September 11, 2001, followed by the anthrax attacks through the U.S. Postal Service, illustrate the vulnerability of the American public to terrorist attacks, including those that use microbes. The key to combating bioterrorist attacks is a highly functioning system of public health surveillance and education that rapidly identifies and effectively contains the attack.

Agents of microbial bioterrorism may be used in their natural form or may be deliberately modified to maximize their deleterious effect. Modifications that increase the deleterious effect of a biologic agent include genetic alteration of microbes to produce antimicrobial resistance, creation of fine-particle aerosols, chemical treatment to stabilize and prolong infectivity, and alteration of the host range through changes in surface protein receptors. Certain of these approaches fall under the category of weaponization, a term that describes the processing of microbes or toxins in a manner that enhances their deleterious effect after release. The key features that characterize an effective biologic weapon are summarized in Table 33-1.



The U.S. Centers for Disease Control and Prevention (CDC) has classified microbial agents that could potentially be used in bioterrorism attacks into three categories: A, B, and C (Table 33-2). Category A agents are the highest-priority pathogens. They pose the greatest risk to national security because they (1) can be easily disseminated or transmitted from person to person, (2) are associated with high case-fatality rates, (3) have potential to cause significant public panic and social disruption, and (4) require special action and public health preparedness.





Anthrax (Bacillus Anthracis)

Anthrax as a Bioweapon Anthrax in many ways is the prototypic bioweapon. Although it is only rarely spread by person-to-person contact, it has many of the other features of an ideal biologic weapon listed in Table 33-1. The potential impact of anthrax as a bioweapon is illustrated by the apparent accidental release in 1979 of anthrax spores from a Soviet bioweapons facility in Sverdlosk, Russia. As a result of this atmospheric release of anthrax spores, at least 77 cases of anthrax (of which 66 were fatal) occurred in individuals within an area 4 km downwind of the facility. Deaths were noted in livestock up to 50 km from the facility. The interval between probable exposure and onset of symptoms ranged from 2 to 43 days, with the majority of cases occurring within 2 weeks. In September of 2001 the American public was exposed to anthrax spores delivered through the U.S. Postal Service. There were 22 confirmed cases: 11 cases of inhaled anthrax (5 died) and 11 cases of cutaneous anthrax (no deaths). Cases occurred in individuals who opened contaminated letters as well as in postal workers involved in processing the mail.

Microbiology and Clinical Features (See also Chaps. 138 and 221, HPIM-18)

• Anthrax is caused by infections with B. anthracis, a gram-positive, nonmotile, spore-forming rod that is found in soil and predominantly causes disease in cattle, goats, and sheep.

• Spores can remain viable for decades in the environment and be difficult to destroy with standard decontamination procedures. These properties make anthrax an ideal bioweapon.

• Naturally occurring human infection generally results from exposure to infected animals or contaminated animal products.

There are three major clinical forms of anthrax:

1. Gastrointestinal anthrax is rare and is unlikely to result from a bioterrorism event.

2. Cutaneous anthrax follows introduction of spores through an opening in the skin. The lesion begins as a papule followed by the development of a black eschar. Prior to the availability of antibiotics, about 20% of cutaneous anthrax cases were fatal.

3. Inhalation anthrax is the form most likely to result in serious illness and death in a bioterrorism attack. It occurs following inhalation of spores that become deposited in the alveolar spaces. The spores are phagocytosed by alveolar macrophages and are transported to regional lymph nodes where they germinate. Following germination, rapid bacterial growth and toxin production occur. Subsequent hematologic dissemination leads to cardiovascular collapse and death. The earliest symptoms are typically those of a viral-like prodrome with fever, malaise, and abdominal/chest symptoms that rapidly progress to a septic shock picture. Widening of the mediastinum and pleural effusions are typical findings on chest radiography. Once considered 100% fatal, experience from the Sverdlosk and U.S. Postal outbreaks indicate that with prompt initiation of appropriate antibiotic therapy, survival may be >50%. Awareness of the possibility of the diagnosis of anthrax is critical to the prompt initiation of therapy.

TREATMENT Anthrax (See Table 33-3)





Anthrax can be successfully treated if the disease is promptly recognized and appropriate antibiotic therapy is initiated.

• Penicillin, ciprofloxacin, and doxycycline are currently licensed for the treatment of anthrax.

• Clindamycin and rifampin have in vitro activity against the organism and may be used as part of the treatment regimen.

• Pts with inhalation anthrax are not contagious and do not require special isolation procedures.

Vaccination and Prevention

• Currently there is a single vaccine licensed for use, produced from a cell-free culture supernatant of an attenuated strain of B. anthracis (Stern strain).

• Current recommendation for postexposure prophylaxis is 60 days of antibiotics (see Table 33-1); recent animal studies have suggested that postexposure vaccination may be of some additional benefit.

Plague (Yersinia Pestis) (See also Chap. 100)

Plague as a Bioweapon Although plague lacks the environmental stability of anthrax, the highly contagious nature of the infection and the high mortality rate make it a potentially important agent of bioterrorism. As a bioweapon, plague would likely be delivered via an aerosol leading to primary pneumonic plague. In such an attack, person-to-person transmission of plague via respiratory aerosol could lead to large numbers of secondary cases.

Microbiology and Clinical Features See Chap. 100.

TREATMENT Plague See Table 33-3 and Chap. 100.

Smallpox (Variola major and V. minor) (See also Chaps. 183 and 221, HPIM-18)

Smallpox as a Bioweapon Smallpox as a disease was globally eradicated by 1980 through a worldwide vaccination program. However, with the cessation of smallpox immunization programs in the United States in 1972 (and worldwide in 1980), close to half the U.S. population is fully susceptible to smallpox today. Given the infectious nature and the 10–30% mortality of smallpox in unimmunized individuals, the deliberate release of virus could have devastating effects on the population. In the absence of effective containment measures, an initial infection of 50–100 persons in a first generation of cases could expand by a factor of 10 to 20 with each succeeding generation. These considerations make smallpox a formidable bioweapon.

Microbiology and Clinical Features The disease smallpox is caused by one of two closely related double-strand DNA viruses, V. major and V. minor. Both viruses are members of the Orthopoxvirus genus of the Poxviridae family. Infection with V. minor is generally less severe, with low mortality rates; thus, V. major is the only one considered as a potential bioweapon. Infection with V. major typically occurs following contact with an infected person from the time that a maculopapular rash appears through scabbing of the pustular lesions. Infection is thought to occur from inhalation of virus-containing saliva droplets from oropharyngeal lesions. Contaminated clothing or linen can also spread infection. About 12–14 days following initial exposure the pt develops high fever, malaise, vomiting, headache, back pain, and a maculopapular rash that begins on the face and extremities and spreads to the trunk. The skin lesions evolve into vesicles that eventually become pustular with scabs. The oral mucosa also develops macular lesions that progress to ulcers. Smallpox is associated with a 10–30% mortality. Historically, about 5–10% of naturally occurring cases manifest as highly virulent atypical forms, classified as hemorrhagic and malignant. These are difficult to recognize due to their atypical manifestations. Both forms have similar onset of a severe prostrating illness characterized by high fever, severe headache, and abdominal and back pain. In the hemorrhagic form, cutaneous erythema develops followed by petechiae and hemorrhage into the skin and mucous membranes. In the malignant form, confluent skin lesions develop but never progress to the pustular stage. Both of these forms are often fatal, with death occurring in 5–6 days.


Treatment is supportive. There is no licensed specific antiviral therapy for smallpox; however, certain candidate drugs look promising in pre-clinical testing in animal models. Smallpox is highly infectious to close contacts; pts who are suspected cases should be handled with strict isolation procedures.

Vaccination and Prevention Smallpox is a preventable disease following immunization with vaccinia. Past and current experience indicates that the smallpox vaccine is associated with a very low incidence of severe complications (see Table 221-4, p. 1775, HPIM-18). The current dilemma facing our society regarding assessment of the risk/benefit of smallpox vaccination is that, while the risks of vaccination are known, the risk of someone deliberately and effectively releasing smallpox into the general population is unknown. Given the rare, but potentially severe complications associated with smallpox vaccination using the currently available vaccine together with the current level of threat, it has been decided by public health authorities that vaccination of the general population is not indicated.

Tularemia (Francisella Tularensis) (See also Chap. 100)

Tularemia as a Bioweapon Tularemia has been studied as a biologic agent since the mid-twentieth century. Reportedly, both the United States and the former Soviet Union had active programs investigating this organism as a possible bioweapon. It has been suggested that the Soviet program extended into the era of molecular biology and that some strains of F. tularensis may have been genetically engineered to be resistant to commonly used antibiotics. F. tularensis is extremely infectious and can cause significant morbidity and mortality. These facts make it reasonable to consider this organism as a possible bioweapon that could be disseminated by either aerosol or contamination of food or drinking water.

Microbiology and Clinical Features See Chap. 100.

TREATMENT Tularemia See Table 33-3 and Chap. 100.

Viral Hemorrhagic Fevers (See also Chap. 113)

Hemorrhagic Fever Viruses as Bioweapons Several of the hemorrhagic fever viruses have been reported to have been weaponized by the former Soviet Union and the United States. Nonhuman primate studies indicate that infection can be established with very few virions and that infectious aerosol preparations can be produced.

Microbiology and Clinical Features See Chap. 113.

TREATMENT Viral Hemorrhagic Fevers See Table 33-3 and Chap. 113.

Botulinum Toxin (Clostridium botulinum) (See also Chap. 101)

Botulinum Toxin as a Bioweapon In a bioterrorism attack, botulinum toxin would likely be dispersed as an aerosol or used to contaminate food. Contamination of the water supply is possible, but the toxin would likely be degraded by chlorine used to purify drinking water. The toxin can also be inactivated by heating food to >85°C for >5 min. The United States, the former Soviet Union, and Iraq have all acknowledged studying botulinum toxin as a potential bioweapon. Unique among the Category A agents for not being a live organism, botulinum toxin is one of the most potent and lethal toxins known to man. It has been estimated that 1 g of toxin is sufficient to kill 1 million people if adequately dispersed.

Microbiology and Clinical Features See Chap. 101.

TREATMENT Botulinum Toxin See Table 33-3 and Chap. 101.


Category B agents are the next highest priority and include agents that are moderately easy to disseminate, produce moderate morbidity and low mortality, and require enhanced diagnostic capacity.

Category C agents are the third highest priority agents in the biodefense agenda. These agents include emerging pathogens, such as SARS (severe acute respiratory syndrome) coronavirus or a pandemic influenza virus, to which the general population lacks immunity. Category C agents could be engineered for mass dissemination in the future. It is important to note that these categories are empirical, and, depending on future circumstances, the priority ratings for a given microbial agent may change.


As indicated above, a diverse array of agents have the potential to be used against a civilian population in a bioterrorism attack. The medical profession must maintain a high index of suspicion that unusual clinical presentations or clustering of rare diseases may not be a chance occurrence, but rather the first sign of a bioterrorism attack. Possible early indicators of a bioterrorism attack could include:

• The occurrence of rare diseases in healthy populations

• The occurrence of unexpectedly large numbers of a rare infection

• The appearance in an urban population of an infectious disease that is usually confined to rural settings

Given the importance of rapid diagnosis and early treatment for many of these diseases, it is important that the medical care team report any suspected cases of bioterrorism immediately to local and state health authorities and/or the CDC (888-246-2675).


The use of chemical warfare agents (CWAs) as weapons of terror against civilian populations is a potential threat that must be addressed by public health officials and the medical profession. The use of both nerve agents and sulfur mustard by Iraq against Iranian military and Kurdish civilians and the sarin attacks in 1994–1995 in Japan underscore this threat.

A detailed description of the various CWAs can be found in Chap. 222, HPIM-18, and on the CDC website at www.bt.cdc.gov/agent/agentlistchem.asp. In this section only vesicants and nerve agents will be discussed, as these are considered the most likely agents to be used in a terrorist attack.


Sulfur mustard is the prototype for this group of CWAs and was first used on the battlefields of Europe in World War I. This agent constitutes both a vapor and liquid threat to exposed epithelial surfaces. The organs most commonly affected are the skin, eyes, and airways. Exposure to large quantities of sulfur mustard can result in bone marrow toxicity. Sulfur mustard dissolves slowly in aqueous media such as sweat or tears, but once dissolved it forms reactive compounds that react with cellular proteins, membranes, and importantly DNA. Much of the biologic damage from this agent appears to result from DNA alkylation and cross-linking in rapidly dividing cells in the corneal epithelium, skin, bronchial mucosal epithelium, GI epithelium, and bone marrow. Sulfur mustard reacts with tissue within minutes of entering the body.

Clinical Features

The topical effects of sulfur mustard occur in the skin, airways, and eyes. Absorption of the agent may produce effects in the bone marrow and GI tract (direct injury to the GI tract may occur if sulfur mustard is ingested in contaminated food or water).

• Skin: erythema is the mildest and earliest manifestation; involved areas of skin then develop vesicles that coalesce to form bullae; high-dose exposure may lead to coagulation necrosis within bullae.

• Airways : initial and, with mild exposures, the only airway manifestations are burning of the nares, epistaxis, sinus pain, and pharyngeal pain. With exposure to higher concentrations, damage to the trachea and lower airways may occur, producing laryngitis, cough, and dyspnea. With large exposures, necrosis of the airway mucosa occurs leading to pseudomembrane formation and airway obstruction. Secondary infection may occur due to bacterial invasion of denuded respiratory mucosa.

• Eyes: the eyes are the most sensitive organ to injury by sulfur mustard. Exposure to low concentrations may produce only erythema and irritation. Exposure to higher concentrations produces progressively more severe conjunctivitis, photophobia, blepharospasm pain, and corneal damage.

• GI tract manifestations include nausea and vomiting, lasting up to 24 h.

• Bone marrow suppression, with peaks at 7–14 days following exposure, may result in sepsis due to leukopenia.

TREATMENT Sulfur Mustard

Immediate decontamination is essential to minimize damage. Immediately remove clothing and gently wash skin with soap and water. Eyes should be flushed with copious amounts of water or saline. Subsequent medical care is supportive. Cutaneous vesicles should be left intact. Larger bullae should be debrided and treated with topical antibiotic preparations. Intensive care similar to that given to severe burn pts is required for pts with severe exposure. Oxygen may be required for mild/moderate respiratory exposure. Intubation and mechanical ventilation may be necessary for laryngeal spasm and severe lower airway damage. Pseudomembranes should be removed by suctioning; bronchodilators are of benefit for bronchospasm. The use of granulocyte colony-stimulating factor and/or stem cell transplantation may be effective for severe bone marrow suppression.


The organophosphorus nerve agents are the deadliest of the CWAs and work by inhibiting synaptic acetylcholinesterase, creating an acute cholinergic crisis. The “classic” organophosphorus nerve agents are tabun, sarin, soman, cyclosarin, and VX. All agents are liquid at standard temperature and pressure. With the exception of VX, all these agents are highly volatile, and the spilling of even a small amount of liquid agent represents a serious vapor hazard.


Inhibition of acetylcholinesterase accounts for the major life-threatening effects of these agents. At the cholinergic synapse, the enzyme acetylcholinesterase functions as a “turn off” switch to regulate cholinergic synaptic transmission. Inhibition of this enzyme allows released acetylcholine to accumulate, resulting in end-organ overstimulation and leading to what is clinically referred to as cholinergic crisis.

Clinical Features

The clinical manifestations of nerve agent exposure are identical for vapor and liquid exposure routes. Initial manifestations include miosis, blurred vision, headache, and copious oropharyngeal secretions. Once the agent enters the bloodstream (usually via inhalation of vapors) manifestations of cholinergic overload include nausea, vomiting, abdominal cramping, muscle twitching, difficulty breathing, cardiovascular instability, loss of consciousness, seizures, and central apnea. The onset of symptoms following vapor exposure is rapid (seconds to minutes). Liquid exposure to nerve agents results in differences in speed of onset and order of symptoms. Contact of a nerve agent with intact skin produces localized sweating followed by localized muscle fasciculations. Once in the muscle, the agent enters the circulation and causes the symptoms described above.

TREATMENT Nerve Agents

Since nerve agents have a short circulating half-life, improvement should be rapid if exposure is terminated and supportive care and appropriate antidotes are given. Thus, the treatment of acute nerve agent poisoning involves decontamination, respiratory support, antidotes.

1. Decontamination: Procedures are the same as those described above for sulfur mustard.

2. Respiratory support: Death from nerve agent exposure is usually due to respiratory failure. Ventilation will be complicated by increased airway resistance and secretions. Atropine should be given before mechanical ventilation is instituted.

3. Antidotal therapy (see Table 33-4):




a. Atropine: Generally the preferred anticholinergic agent of choice for treating acute nerve agent poisoning. Atropine rapidly reverses cholinergic overload at muscarinic synapses but has little effect at nicotinic synapses. Thus, atropine can rapidly treat the life-threatening respiratory effects of nerve agents but will probably not help neuromuscular effects. The field loading dose is 2–6 mg IM, with repeat doses given every 5–10 min until breathing and secretions improve. In the mildly affected pt with miosis and no systemic symptoms, atropine or homoatropine eye drops may suffice.

b. Oxime therapy: Oximes are nucleophiles that help restore normal enzyme function by reactivating the cholinesterase whose active site has been occupied and bound by the nerve agent. The oxime available in the United States is 2-pralidoxime chloride (2-PAM Cl). Treatment with 2-PAM may cause blood pressure elevation.

c. Anticonvulsant: Seizures caused by nerve agents do not respond to the usual anticonvulsants such as phenytoin, phenobarbital, carbamazepine, valproate, and lamotrigine. The only class of drugs known to have efficacy in treating nerve agent–induced seizures are the benzodiazepines. Diazepam is the only benzodiazepine approved by the U.S. Food and Drug Administration for the treatment of seizures (although other benzodiazepines have been shown to work well in animal models of nerve agent–induced seizures).


Nuclear or radiation-related devices represent a third category of weapon that could be used in a terrorism attack. There are two major types of attacks that could occur. The first is the use of radiologic dispersal devices that cause the dispersal of radioactive material without detonation of a nuclear explosion. Such devices could use conventional explosives to disperse radio-nuclides. The second, and less probable, scenario would be the use of actual nuclear weapons by terrorists against a civilian target. In addition to weaponization, detrimental human exposure has also resulted from unintentional breaches in radiation containment. The consequences of radiation sickness remain the same for accidental exposure as they do for deliberate release.


Alpha radiation consists of heavy, positively charged particles containing two protons and two neutrons. Due to their large size, alpha particles have limited penetrating power. Cloth and human skin can usually prevent alpha particles from penetrating into the body. If alpha particles are internalized, they can cause significant cellular damage.

Beta radiation consists of electrons and can travel only short distances in tissue. Plastic layers and clothing can stop most beta particles. Higher energy beta particles can cause injury to the basal stratum of skin similar to a thermal burn.

Gamma radiation and x-rays are forms of electromagnetic radiation discharged from the atomic nucleus. Sometimes referred to as penetrating radiation, both gamma and x-rays easily penetrate matter and are the principle type of radiation to cause whole-body exposure (see below).

Neutron particles are heavy and uncharged; often emitted during a nuclear detonation. Their ability to penetrate tissues is variable, depending upon their energy. They are less likely to be generated in various scenarios of radiation bioterrorism.

The commonly used units of radiation are the rad and the gray. The rad is the energy deposited within living matter and is equal to 100 ergs/g of tissue. The rad has been replaced by the SI unit of the gray (Gy). 100 rad = 1 Gy.


Whole-body exposure represents deposition of radiation energy over the entire body. Alpha and beta particles have limited penetration power and do not cause significant whole-body exposure unless they are internalized in large amounts. Whole-body exposure from gamma rays, x-rays, or high-energy neutron particles can penetrate the body, causing damage to multiple tissues and organs.

External contamination results from fallout of radioactive particles landing on the body surface, clothing, and hair. This is the dominant form of contamination likely to occur in a terrorist strike that utilizes a dispersal device. The most likely contaminants would emit alpha and beta radiation. Alpha particles do not penetrate the skin and thus would produce minimal systemic damage. Beta emitters can cause significant cutaneous burns. Gamma emitters not only cause cutaneous burns but can also cause significant internal damage.

Internal contamination will occur when radioactive material is inhaled, is ingested, or is able to enter the body via a disruption in the skin. The respiratory tract is the main portal of entrance for internal contamination, and the lung is the organ at greatest risk. Radioactive material entering the GI tract will be absorbed according to its chemical structure and solubility. Penetration through the skin usually occurs when wounds or burns have disrupted the cutaneous barrier. Absorbed radioactive materials will travel throughout the body. Liver, kidney, adipose tissue, and bone tend to bind and retain radioactive material more than do other tissues.

Localized exposure results from close contact between highly radioactive material and a part of the body, resulting in discrete damage to the skin and deeper structures.


Radiation interactions with atoms can result in ionization and free radical formation that damages tissue by disrupting chemical bonds and molecular structures in the cell, including DNA. Radiation can lead to cell death; cells that recover may have DNA mutations that pose a higher risk for malignant transformation. Cell sensitivity to radiation damage increases as replication rate increases. Bone marrow and mucosal surfaces in the GI tract have high mitotic activity and thus are significantly more prone to radiation damage than slowly dividing tissues such as bone and muscle. Acute radiation sickness (ARS) can develop following exposure of all or most of the human body to ionizing radiation. The clinical manifestations of ARS reflect the dose and type of radiation as well as the parts of the body that are exposed.

Clinical Features

ARS produces signs and symptoms related to damage of three major organ systems: GI tract, bone marrow, and neurovascular. The type and dose of radiation and the part of the body exposed will determine the dominant clinical picture.

• There are four major stages of ARS:

1. Prodrome occurs between hours to 4 days after exposure and lasts from hours to days. Manifestations include nausea, vomiting, anorexia, and diarrhea.

2. The latent stage follows the prodrome and is associated with minimal or no symptoms. It most commonly lasts up to 2 weeks, but can last as long as 6 weeks.

3. Illness follows the latent stage.

4. Death or recovery is the final stage of ARS.

• The higher the radiation dose, the shorter and more severe the stage.

• At low radiation doses (0.7–4 Gy), bone marrow suppression occurs and constitutes the main illness. The pt may develop bleeding or infection secondary to thrombocytopenia and leukopenia. The bone marrow will generally recover in most pts. Care is supportive (transfusion, antibiotics, colony-stimulating factors).

• With exposure to 6–8 Gy, the clinical picture is more complicated; the bone marrow may not recover and death will ensue. Damage to the GI mucosa producing diarrhea, hemorrhage, sepsis, fluid and electrolyte imbalance may occur and complicate the clinical picture.

• Whole-body exposure to >10 Gy is usually fatal. In addition to severe bone marrow and GI tract damage, a neurovascular syndrome characterized by vascular collapse, seizures, and death may occur (especially at doses >20 Gy).

TREATMENT Acute Radiation Sickness

Treatment of ARS is largely supportive (Fig. 33-1).


FIGURE 33-1 General guidelines for treatment of radiation casualties. CBC, complete blood count.

1. Persons contaminated either externally or internally should be decontaminated as soon as possible. Contaminated clothes should be removed; showering or washing the entire skin and hair is very important. A radiation detector should be used to check for residual contamination. Decontamination of medical personnel should occur following emergency treatment and decontamination of the pt.

2. Treatment for the hematopoietic system includes appropriate therapy for neutropenia and infection, transfusion of blood products as needed, and hematopoietic growth factors. The value of bone marrow transplantation in this situation is unknown.

3. Partial or total parenteral nutrition is appropriate supportive therapy for pts with significant injury to the GI mucosa.

4. Treatment of internal radionuclide contamination is aimed at reducing absorption and enhancing elimination of the ingested material (Table 223-2, p. 1794, HPIM-18).

a. Clearance of the GI tract may be achieved by gastric lavage, emetics, or purgatives, laxatives, ion exchange resins, and aluminum-containing antacids.

b. Administration of blocking agents is aimed at preventing the entrance of radioactive materials into tissues (e.g., potassium iodide, which blocks the uptake of radioactive iodine by the thyroid).

c. Diluting agents decrease the absorption of the radionuclide (e.g., water in the treatment of tritium contamination).

d. Mobilizing agents are most effective when given immediately; however, they may still be effective for up to 2 weeks following exposure. Examples include antithyroid drugs, glucocorticoids, ammonium chloride, diuretics, expectorants, and inhalants. All of these should induce the release of radionuclides from tissues.

e. Chelating agents bind many radioactive materials, after which the complexes are excreted from the body.


For a more detailed discussion, see Lane HC, Fauci AS: Microbial Bioterrorism, Chap. 221, p. 1768; Hurst CG, Newmark J, Romano JA: Chemical Terrorism, Chap. 222, p. 1779; and Tochner ZA, Glatstein E: Radiation Terrorism, Chap. 223, p. 1788, in HPIM-18.